Protection from hypoxic injuries that cause cardiopulmonary and cerebral dysfunction is a focus of current clinical research. A decline in β-adrenergic receptors and P2-purinergic receptors in cardiopulmonary and cerebral vascular systems, superoxide anion-induced endothelial injuries, and elevated intracellular calcium influx are key factors leading to cardiopulmonary and cerebral injuries. Pharmacotherapies using verapamil, isoprenaline, or superoxide dismutase alone for targeting the key loops of cardiopulmonary and cerebral hypoxic injuries have demonstrated low efficacy and high toxicity.